Evidence map›Paper›PMID 20448056›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

p53 mediates cigarette smoke-induced apoptosis of pulmonary endothelial cells: inhibitory effects of macrophage migration inhibitor factor.

Rachel Damico, Tiffany Simms, Bo S Kim, Zenar Tekeste, Henry Amankwan, Mahendra Damarla, Paul M Hassoun

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
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  7. Review
  8. Review
  9. Review
  10. Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.American journal of respiratory cell and molecular biology · 2020
    Article
  11. Article
  12. Article
  13. Functional Impact of Human Genetic Variants ofAmerican journal of respiratory cell and molecular biology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury.Advances in anatomy, embryology, and cell biology · 2018
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Rachel DamicoDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA. rdamico1@jhmi.edu
Tiffany Simms
Bo S Kim
Zenar Tekeste
Henry Amankwan
Mahendra Damarla
Paul M Hassoun
Johns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to cigarette smoke (CS) is the most common cause of emphysema, a debilitating pulmonary disease histopathologically characterized by the irreversible destruction of lung architecture. Mounting evidence links enhanced endothelial apoptosis causally to the development of emphysema. However, the molecular determinants of human endothelial cell apoptosis and survival in response to CS are not fully defined. Such determinants could represent clinically relevant targets for intervention. We show here that CS extract (CSE) triggers the death of human pulmonary macrovascular endothelial cells (HPAECs) through a caspase 9-dependent apoptotic pathway. Exposure to CSE results in the increased expression of p53 in HPAECs. Using the p53 inhibitor, pifithrin-α (PFT-α), and RNA interference (RNAi) directed at p53, we demonstrate that p53 function and expression are required for CSE-mediated apoptosis. The expression of macrophage migration inhibitory factor (MIF), an antiapoptotic cytokine produced by HPAECs, also increases in response to CSE exposure. The addition of recombinant human MIF prevents cell death from exposure to CSE. Further, the suppression of MIF or its receptor/binding partner, Jun activation domain-binding protein 1 (Jab-1), with RNAi enhances the sensitivity of human pulmonary endothelial cells to CSE via a p53-dependent (PFT-α-inhibitable) pathway. Finally, we demonstrate that MIF is a negative regulator of p53 expression in response to CSE, placing MIF upstream of p53 as an antagonist of CSE-induced apoptosis. We conclude that MIF can protect human vascular endothelium from the toxic effects of CSE via the antagonism of p53-mediated apoptosis.

Indexed as

Gene Expression RegulationApoptosisCaspase 9Cells, CulturedCOP9 Signalosome ComplexEndothelial CellsHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsLungMacrophage Migration-Inhibitory FactorsPeptide HydrolasesRNA InterferenceRNA, Small InterferingSmokingTumor Suppressor Protein p53Caspase 9COP9 Signalosome ComplexCOPS5 protein, humanIntracellular Signaling Peptides and ProteinsMacrophage Migration-Inhibitory FactorsPeptide HydrolasesRNA, Small InterferingTumor Suppressor Protein p53

Identifiers

PMID20448056
PMCPMC3095933
OpenAlexW1911955986

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.